The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Mitochondrial dysfunction and oxidative stress in Parkinson's disease and monogenic parkinsonism
Open accessAbstract
The pathogenic mechanisms that underlie Parkinson’s disease remain unknown. Here, we review evidence from both sporadic and genetic forms of Parkinson’s disease that implicate both mitochondria and oxidative stress as central players in disease pathogenesis. A systemic deficiency in complex I of the mitochondrial electron transport chain is evident in many patients with the disease. Oxidative stress caused by reactive metabolites of dopamine and alterations in the levels of iron and glutathione in the substantia nigra accompany this mitochondrial dysfunction. Recent evidence from studies on the genetic forms of parkinsonism with particular stress on DJ-1, parkin, and PINK-1 also suggest the involvement of mitochondria and oxidative stress.
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Citations
Cites
Staging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777
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Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
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Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
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Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
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PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
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“Neurons are thought to rely more on astrocyte derived lactate as substrates for oxidative phosphorylation, but they continue to be dependent on mitochondrial function for survival (Pellerin and Magistretti, 1994; Wyss et al., 2011).”
BackgroundPINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
Geisler, S., Holmström, K. M., Skujat, D., Fiesel, F. C., Rothfuss, O. C., Kahle, P. J., & Springer, W. (2010) · Nature Cell Biology · doi:10.1038/ncb2012 · Cited by 2,835
Premature ageing in mice expressing defective mitochondrial DNA polymerase
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Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging
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Cited by
The role of oxidative stress in neurodegenerative diseases
Kim, G. H., Kim, J. E., Rhie, S. J., & Yoon, S. (2015) · Experimental Neurobiology · doi:10.5607/en.2015.24.4.325 · Cited by 1,355
Dopamine: Functions, Signaling, and Association with Neurological Diseases
Klein, M. O., Battagello, D. S., Cardoso, A. R., Hauser, D. N., Bittencourt, J. C., & Correa, R. G. (2019) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-018-0632-3 · Cited by 1,073
Self-citationDeubiquitylating enzymes and drug discovery: emerging opportunities
Harrigan, J. A., Jacq, X., Martin, N. M., & Jackson, S. P. (2018) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2017.152 · Cited by 940
Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives
Hajam, Y. A., Rani, R., Ganie, S. Y., Sheikh, T. A., Javaid, D., Qadri, S. S., Pramodh, S., Alsulimani, A., Alkhanani, M. F., Harakeh, S., et al. (2022) · Cells · doi:10.3390/cells11030552 · Cited by 915
The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy
Bingol, B., Tea, J. S., Phu, L., Reichelt, M., Bakalarski, C. E., Song, Q., Foreman, O., Kirkpatrick, D. S., & Sheng, M. (2014) · Nature · doi:10.1038/nature13418 · Cited by 855
Metadata
- Authors
- Hauser, D. N., & Hastings, T. G.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2013-03
- Volume
- 51
- Pages
- 35-42
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W1963577160
- Cited by
- 474
- References
- 24
- FWCI
- 20.57
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
